RGD Reference Report - Phosphatase-mediated crosstalk between MAPK signaling pathways in the regulation of cell survival. - Rat Genome Database

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Phosphatase-mediated crosstalk between MAPK signaling pathways in the regulation of cell survival.

Authors: Junttila, MR  Li, SP  Westermarck, J 
Citation: Junttila MR, etal., FASEB J. 2008 Apr;22(4):954-65. Epub 2007 Nov 26.
RGD ID: 5129956
Pubmed: PMID:18039929   (View Abstract at PubMed)
DOI: DOI:10.1096/fj.06-7859rev   (Journal Full-text)

Mitogen-activated protein kinase (MAPK) pathways constitute a large modular network that regulates a variety of physiological processes, such as cell growth, differentiation, and apoptotic cell death. The function of the ERK pathway has been depicted as survival-promoting, in essence by opposing the proapoptotic activity of the stress-activated c-Jun NH(2)-terminal kinase (JNK)/p38 MAPK pathways. However, recently published work suggests that extracellular regulated kinase (ERK) pathway activity is suppressed by JNK/p38 kinases during apoptosis induction. In this review, we will summarize the current knowledge about JNK/p38-mediated mechanisms that negatively regulate the ERK pathway. In particular, we will focus on phosphatases (PP2A, MKPs) as inhibitors of ERK pathway activity in regulating apoptosis. A model proposed in this review places the negative regulation of the ERK pathway in a central position for the cellular decision-making process that determines whether cells will live or die in response to apoptosis-promoting signals. In addition, we will discuss the potential functional relevance of negative regulation of ERK pathway activity, for physiological and pathological conditions (e.g., cellular transformation).


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